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Mechanical, electrical and cyclic nucleotide responses to peptide VIP and inhibitory nerve stimulation in rat stomach.
Author(s) -
Ito S,
Kurokawa A,
Ohga A,
Ohta T,
Sawabe K
Publication year - 1990
Publication title -
the journal of physiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.802
H-Index - 240
eISSN - 1469-7793
pISSN - 0022-3751
DOI - 10.1113/jphysiol.1990.sp018294
Subject(s) - apamin , vasoactive intestinal peptide , endocrinology , medicine , stimulation , tetrodotoxin , guanethidine , antrum , hyperpolarization (physics) , inhibitory postsynaptic potential , chemistry , biology , neuropeptide , stomach , potassium channel , receptor , organic chemistry , nuclear magnetic resonance spectroscopy
1. Effects of apamin on electrical and mechanical activities and cyclic nucleotide accumulation in response to vasoactive intestinal peptide (VIP) and intramural nerve stimulation were investigated in isolated circular strips of the rat stomach in the presence of atropine and guanethidine. 2. Circular muscles generated rhythmic contractions and slow waves in the antrum but not in the fundus. Intramural nerve stimulation and VIP caused frequency‐ and dose‐dependent relaxation of fundic strips and inhibition of spontaneous contractions of antral strips. Apamin partly reduced the responses to intramural nerve stimulation but not those to VIP. 3. In the antrum, apamin reduced inhibitory junction potentials (IJPs) evoked at the nadir of slow waves but not at their zenith. In the fundus, apamin partly decreased the amplitude of IJPs. Repetitive nerve stimulation was associated with an apamin‐sensitive hyperpolarization and apamin‐resistant decrease in the slow wave amplitude in the antrum. 4. VIP caused a dose‐dependent hyperpolarization of fundic circular muscle membrane. In the antrum, VIP inhibited spike potentials superimposed on slow waves and it decreased the slow wave amplitude in about half of the preparations. These electrical responses to VIP were resistant to apamin. 5. Intramural nerve stimulation evoked an apamin‐resistant output of VIP from muscle strips, which no longer occurred after tetrodotoxin or removal of extracellular Ca2+. 6. Intramural nerve stimulation and VIP elicited apamin‐resistant increases in cyclic AMP and cyclic GMP accumulations. The effects of VIP on cyclic AMP were greater than those on cyclic GMP. The effects of intramural nerve stimulation on cyclic GMP were faster in onset than those of cyclic AMP. 7. It is suggested that VIP is a neurotransmitter of the intramural inhibitory nerves concerned in the apamin‐resistant relaxation of the rat stomach.